030 Brain aging and cardiovascular risk factors in chronic HIV: A longitudinal MRI study

D. Jakabek, C. Rae, B. Brew, L. Cysique
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Abstract

Objectives We aimed to examine the relative contributions of HIV infection, age, and cardiovascular risk factors to subcortical brain atrophy. Methods Virally suppressed HIV+ participants with low neuropsychological confounds (n = 75) and demographically matched HIV- controls (n = 31) completed baseline and 18-month follow-up MRI scans, neuropsychological evaluation, cardiovascular assessments, and laboratory tests. HIV+ participants were evaluated for HIV associated neurocognitive disorder (HAND). Subcortical volumes were extracted with Freesurfer. Volumetric and shape analyses were conducted using linear mixed-effect models incorporating interactions between age, time, and each of HIV status, HAND status, HIV disease factors, and cardiovascular markers. Results HIV+ participants had smaller volumes of most structures compared to HIV- participants. Premature aging was evident in the pallidum using volumetric (p = 0.032) and shape analyses. Accelerated aging was observed in the caudate volumes for the more severe HAND subgroup (p = 0.008) and was associated with longer HIV duration for putamen volumes (p = 0.04). Higher CD4 counts had a protective effect on hippocampal volumes in older participants (p = 0.04). Cardiovascular measures were associated with smaller volumes across time for most structures; only the putamen demonstrated accelerated atrophy over time in HIV+ participants with higher cardiovascular risk factors (p = 0.002). Conclusion The study demonstrates a three-hit model of subcortical injury in HIV+ individuals: HIV-driven atrophy in most subcortical structures; abnormal brain aging and HIV infection synergy in the caudate and pallidum; and cardiovascular-related injury linked to diffuse premature atrophy and emerging accelerated atrophy in the putamen.
慢性HIV患者脑老化和心血管危险因素:纵向MRI研究
目的:研究HIV感染、年龄和心血管危险因素对皮质下脑萎缩的影响。方法病毒抑制的HIV阳性低神经心理混杂的参与者(n = 75)和人口统计学上匹配的HIV对照组(n = 31)完成了基线和18个月的随访MRI扫描、神经心理评估、心血管评估和实验室检查。HIV阳性参与者评估HIV相关神经认知障碍(HAND)。用Freesurfer提取皮质下体积。使用线性混合效应模型进行体积和形状分析,该模型结合了年龄、时间、HIV状态、HAND状态、HIV疾病因素和心血管标志物之间的相互作用。结果HIV阳性受试者的大部分结构体积比HIV阳性受试者小。使用体积(p = 0.032)和形状分析,苍白球明显过早老化。更严重的HAND亚组在尾状核体积中观察到加速老化(p = 0.008),并且与壳核体积中更长的HIV持续时间相关(p = 0.04)。较高的CD4计数对老年参与者的海马体积有保护作用(p = 0.04)。随着时间的推移,大多数结构的心血管测量与较小的体积相关;在心血管危险因素较高的HIV阳性参与者中,只有壳核随着时间的推移加速萎缩(p = 0.002)。结论本研究证实了HIV+个体皮层下损伤的三击模型:HIV驱动的大部分皮层下结构萎缩;脑异常老化与HIV感染在尾状和苍白质中的协同作用;心血管相关损伤与弥漫性过早萎缩和壳核出现的加速萎缩有关。
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